We will continue to explore the relationship between mitochondrial ion flux and control of gluconeogenesis. More specifically, we will test the hypothesis that the ability of organic cations to stimulate the initial rate of energized Ca2 ion uptake hepatic mitochondria is the parameter which correlates with inhibition of glucagon-stimulated hepatic gluconeogenesis in the intact liver or hypoglycemia in the whole animal. The kinetics of accelerated initial Ca2 ion uptake rate into mitochondria will be investigated in detail. We will also attempt to affinity-label the guanidinium binding site of mitochondria using 4-phenyl-3,5-dimethylpyrazole-(C14)-1-carboxamidine. BIBLIOGRAPHIC REFERENCES: Koncz, L., DeLellis, R.A., Zimmerman, C., Franklin, A. and Davidoff, F., The spleen as transplant site for islets in diabetic rats, Diabetes (Abstract) 24:437 (1975). Koncz, L., Davidoff, F., DeLellis, R.A., Selby, M., and Zimmerman, C.E., Quantiative aspects of the metabolic response to pancreatic islet transplantation in rats with severe ketotic diabetes, Metabolism, 25:147-156 (1976).